Effects of chronically high levels of aldosterone on different cognitive dimensions: an investigation in patients with primary aldosteronism.

Primary aldosteronism is a natural model for chronic aldosterone excess in humans and associated with symptoms of anxiety and depression. Cognitive deficits are inherent to the symptomatology of depression and anxiety disorders. Mineralocorticoid receptors and aldosterone appear to play a role in memory. Aldosterone was additionally supposed to be a risk factor for cognitive decline in patients with essential hypertension. The objective of this study was to investigate possible effects of chronically high aldosterone concentrations on cognitive function. A range of cognitive dimensions were assessed in 19 patients (9 males, 10 females); mean age 47.1 (12.5) under standardized treatment and several rating scales for anxiety, depression, quality of life and sleep were administered. Cognitive parameters were compared to standard norms from a large, healthy standardization sample. Patients showed increased levels of anxiety and depression without meeting diagnostic criteria for a disorder. Besides a numerically lower attention score, patients did not show any significant differences in the cognitive dimensions. Anxiety and depression were negatively correlated with quantitative performance in males. In females, a negative correlation between sleep disturbances and abstract reasoning and a positive correlation with quantitative performance were found. Our data showed no specific effect of chronic aldosterone in the tested cognitive parameters overall at least in younger patients, but they indicate sexually dimorphic regulation processes.

Sleep-EEG in patients with primary aldosteronism in comparison to healthy controls and patients with depression.

The mineralocorticoid receptor (MR)/glucocorticoid receptor balance plays an important role in the pathophysiology of anxiety and depression. Aldosterone, a primary MR ligand, seems to be related to the pathophysiology of anxiety and depressive symptoms. The objective of this study was to investigate effects of aldosterone excess on sleep EEG, as sleep EEG is a tool to gain insight into psychoneuroendocrine function. Here, 19 untreated patients (9 males, 10 females) suffering from primary aldosteronism were investigated using sleep EEG and several rating scales for anxiety, depression, quality of life and sleep before starting specific treatment. Parameters were compared to age and sex matched healthy controls and patients with depression and correlated with laboratory findings and blood pressure. Patients had higher values for anxiety and depression compared to the general population, although a psychiatric disorder in their history was ruled out. Although sleep disturbances were reported in the Pittsburgh sleep quality index, sleep EEG did not show significant changes between patients and healthy controls. No depression specific pattern in sleep EEG was found. But in contrast to females, several sleep-EEG parameters of male PA patients differed significantly from patients with depression. There was a significant correlation between blood pressure and the severity of depression and anxiety in females. Correlation analysis between blood pressure and rating scales indicate a relationship between blood pressure and anxiety in women. In conclusion, these data suggest gender related effects of aldosterone excess in males and females.